Inhibition of tumour cell growth by carnosine: some possible mechanisms

Alan R. Hipkiss*, Frank Gaunitz

*Corresponding author for this work

Research output: Contribution to journalArticle

Abstract

The naturally occurring dipeptide carnosine (β-alanyl-l-histidine) has been shown to inhibit, selectively, growth of transformed cells mediated, at least in part, by depleting glycolytic ATP levels. The mechanism(s) responsible has/have yet to be determined. Here, we discuss a number of probable and/or possible processes which could, theoretically, suppress glycolytic activity which would decrease ATP supply and generation of metabolic intermediates required for continued cell reproduction. Possibilities include effects on (i) glycolytic enzymes, (ii) metabolic regulatory activities, (iii) redox biology, (iv) protein glycation, (v) glyoxalase activity, (vi) apoptosis, (vii) gene expression and (viii) metastasis. It is possible, by acting at various sites that this pluripotent dipeptide may be an example of an endogenous "smart drug".

Original languageEnglish
Pages (from-to)327-337
Number of pages11
JournalAmino Acids
Volume46
Issue number2
Early online date1 Dec 2013
DOIs
Publication statusPublished - 1 Feb 2014

Fingerprint

Carnosine
Dipeptides
Cell growth
Tumors
Adenosine Triphosphate
Growth
Histidine
Gene expression
Oxidation-Reduction
Reproduction
Neoplasms
Apoptosis
Neoplasm Metastasis
Gene Expression
Enzymes
Pharmaceutical Preparations
Proteins

Keywords

  • cancer
  • carnosine
  • glycation
  • glycolysis
  • metastasis
  • NAD
  • Redox biology
  • regulation
  • signalling
  • tumour

Cite this

Hipkiss, Alan R. ; Gaunitz, Frank. / Inhibition of tumour cell growth by carnosine : some possible mechanisms. In: Amino Acids. 2014 ; Vol. 46, No. 2. pp. 327-337.
@article{409b7ec31ea44528bddfed5bca2aa2bc,
title = "Inhibition of tumour cell growth by carnosine: some possible mechanisms",
abstract = "The naturally occurring dipeptide carnosine (β-alanyl-l-histidine) has been shown to inhibit, selectively, growth of transformed cells mediated, at least in part, by depleting glycolytic ATP levels. The mechanism(s) responsible has/have yet to be determined. Here, we discuss a number of probable and/or possible processes which could, theoretically, suppress glycolytic activity which would decrease ATP supply and generation of metabolic intermediates required for continued cell reproduction. Possibilities include effects on (i) glycolytic enzymes, (ii) metabolic regulatory activities, (iii) redox biology, (iv) protein glycation, (v) glyoxalase activity, (vi) apoptosis, (vii) gene expression and (viii) metastasis. It is possible, by acting at various sites that this pluripotent dipeptide may be an example of an endogenous {"}smart drug{"}.",
keywords = "cancer, carnosine, glycation, glycolysis, metastasis, NAD, Redox biology, regulation, signalling, tumour",
author = "Hipkiss, {Alan R.} and Frank Gaunitz",
year = "2014",
month = "2",
day = "1",
doi = "10.1007/s00726-013-1627-5",
language = "English",
volume = "46",
pages = "327--337",
journal = "Amino Acids",
issn = "0939-4451",
publisher = "Springer",
number = "2",

}

Inhibition of tumour cell growth by carnosine : some possible mechanisms. / Hipkiss, Alan R.; Gaunitz, Frank.

In: Amino Acids, Vol. 46, No. 2, 01.02.2014, p. 327-337.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Inhibition of tumour cell growth by carnosine

T2 - some possible mechanisms

AU - Hipkiss, Alan R.

AU - Gaunitz, Frank

PY - 2014/2/1

Y1 - 2014/2/1

N2 - The naturally occurring dipeptide carnosine (β-alanyl-l-histidine) has been shown to inhibit, selectively, growth of transformed cells mediated, at least in part, by depleting glycolytic ATP levels. The mechanism(s) responsible has/have yet to be determined. Here, we discuss a number of probable and/or possible processes which could, theoretically, suppress glycolytic activity which would decrease ATP supply and generation of metabolic intermediates required for continued cell reproduction. Possibilities include effects on (i) glycolytic enzymes, (ii) metabolic regulatory activities, (iii) redox biology, (iv) protein glycation, (v) glyoxalase activity, (vi) apoptosis, (vii) gene expression and (viii) metastasis. It is possible, by acting at various sites that this pluripotent dipeptide may be an example of an endogenous "smart drug".

AB - The naturally occurring dipeptide carnosine (β-alanyl-l-histidine) has been shown to inhibit, selectively, growth of transformed cells mediated, at least in part, by depleting glycolytic ATP levels. The mechanism(s) responsible has/have yet to be determined. Here, we discuss a number of probable and/or possible processes which could, theoretically, suppress glycolytic activity which would decrease ATP supply and generation of metabolic intermediates required for continued cell reproduction. Possibilities include effects on (i) glycolytic enzymes, (ii) metabolic regulatory activities, (iii) redox biology, (iv) protein glycation, (v) glyoxalase activity, (vi) apoptosis, (vii) gene expression and (viii) metastasis. It is possible, by acting at various sites that this pluripotent dipeptide may be an example of an endogenous "smart drug".

KW - cancer

KW - carnosine

KW - glycation

KW - glycolysis

KW - metastasis

KW - NAD

KW - Redox biology

KW - regulation

KW - signalling

KW - tumour

UR - http://www.scopus.com/inward/record.url?scp=84895911229&partnerID=8YFLogxK

U2 - 10.1007/s00726-013-1627-5

DO - 10.1007/s00726-013-1627-5

M3 - Article

C2 - 24292217

AN - SCOPUS:84895911229

VL - 46

SP - 327

EP - 337

JO - Amino Acids

JF - Amino Acids

SN - 0939-4451

IS - 2

ER -